@Article{096504016X14772349843854,
AUTHOR = {Li-Zhou Fang, Jian-Qing Zhang, Ling Liu, Wei-Ping Fu, Jing-Kui Shu, Jia-Gang Feng, Xiao Liang},
TITLE = {Silencing of Btbd7 Inhibited Epithelial–Mesenchymal Transition  and Chemoresistance in CD133<sup>+</sup> Lung Carcinoma A549 Cells},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {5},
PAGES = {819--829},
URL = {http://www.techscience.com/or/v25n5/56864},
ISSN = {1555-3906},
ABSTRACT = {Cancer stem cells (CSCs) are responsible for tumorigenesis and recurrence, so targeting CSCs is an effective 
method to potentially cure cancer. BTB/POZ domain-containing protein 7 (Btbd7) has been found in various 
cancers, including lung cancer and liver cancer, but the role of Btbd7 in non-small cell lung cancer (NSCLC), 
CSC self-renewal, and chemoresistance is still unknown. Therefore, in this study we found that the ratio of 
tumor sphere formation and stem cell transcription factors in CD133<sup>+</sup>
 cells was dramatically enhanced compared to parental cells, which indicated successful sorting of CD133<sup>+</sup>
 cells from A549. Meanwhile, Btbd7 and 
the markers of the epithelial–mesenchymal transition (EMT) process were more highly expressed in CD133<sup>+</sup>
cells than in parental cells. Silencing of Btbd7 significantly inhibited the self-renewal and EMT process in 
CD133<sup>+</sup>
 cells. Furthermore, we found that downregulation of Btbd7 promoted cell apoptosis and increased the 
sensitivity to paclitaxel in CD133<sup>+</sup>
 and parental cells. In conclusion, our results suggest that Btbd7 is a promising agent for the inhibition of survival and chemoresistance of cancer stem-like cells of NSCLC, which may 
act as an important therapeutic target in NSCLC.},
DOI = {10.3727/096504016X14772349843854}
}